Ginsenoside Rg3 inhibits angiotensin II-induced cardiac fibrosis via the glucagon-like peptide-1 receptor signaling pathway

Key Result

Ginsenoside Rg3 suppressed collagen deposition and reduced fibrosis-related proteins in Ang II-infused mice by inhibiting RhoA/ROCK and Smad2/3 pathways via GLP-1R upregulation.

Key Points

• This research aims to investigate the role of ginsenoside Rg3 in preventing cardiac fibrosis and its underlying molecular mechanisms.
• Utilized cardiac fibrosis models to assess the effects of Rg3.
• Monitored activation of RhoA/ROCK and Smad2/3 pathways.
• Measured levels of GLP-1 receptor (GLP-1R) expression.
• Rg3 significantly inhibited the activation of RhoA/ROCK and Smad2/3 pathways.
• There was a notable upregulation of GLP-1R in response to Rg3 treatment.
• The anti-fibrotic effect was confirmed through histological assessments.